The exact mechanisms leading to increased uterine tone resulting in preterm labor or uterine hypertonus have not been elucidated. The most important pathways producing uterine contraction and relaxation are OT and bAR-mediated pathways. The goals of the proposal are to understand the interactions between these two pathways in non pregnant myometrium, how pregnancy affects this interaction and how interaction between pathways affects responses to changes in bAR activity. These studies will be performed in a fresh and cultured pregnant and non pregnant rat and human myometrium, pretreated with OT. Studies will include measurement of numbers and affinities of bAR and OT receptors and AC activity. To identify the role of specific isoforms of AC, they will determine presence and quantities of protein and mRNA for those isoforms involved in the desensitization of AC. The knowledge of the interaction between signal transducing pathways causing uterine hyperactivity will lead to prevention of fetal distress and preterm labor and uterine hypertonus.